期刊
JOURNAL OF INFECTIOUS DISEASES
卷 206, 期 4, 页码 552-561出版社
OXFORD UNIV PRESS INC
DOI: 10.1093/infdis/jis379
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资金
- Oxford NIHR Biomedical Research Centre
- Medical Research Council UK
- National 12th Five-Year Major Projects of China [2012ZX10001-003, 2012ZX10001-006]
- Beijing Municipal Science and Technology Committee [D09050703590901]
- Medical Research Council [MC_U137884177, G0502048] Funding Source: researchfish
- MRC [MC_U137884177, G0502048] Funding Source: UKRI
Background. Rare human immunodeficiency virus type 1 (HIV-1)-infected individuals who maintain control of viremia without therapy show potent CD8+ T-cell-mediated suppression of viral replication in vitro. Whether this is a determinant of the rate of disease progression in viremic individuals is unknown. Methods. We measured CD8+ T-cell-mediated inhibition of a heterologous HIV-1 isolate in 50 HIV-1-seropositive adults with diverse progression rates. Linear mixed models were used to determine whether CD8+ T-cell function could explain variation in the rate of CD4+ T-cell decline. Results. There was a significant interaction between CD8+ T-cell antiviral activity in vitro and the rate of CD4+ T-cell decline in chronically infected individuals (P < .0001). In a second prospective analysis of recently infected subjects followed for up to 3 years, CD8+ T-cell antiviral activity strongly predicted subsequent CD4+ T-cell decline (P < .0001) and explained up to 73% of the interindividual variation in the CD4+ T-cell slope. In addition, it was inversely associated with viral load set point (r = -0.68 and P = .002). Conclusions. The antiviral inhibitory capacity of CD8+ T cells is highly predictive of CD4+ T-cell loss in early HIV-1 infection. It has potential as a benchmark of effective immunity in vaccine evaluation.
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